Issue 40

I. Doulamis et alii, Frattura ed Integrità Strutturale, 40 (2017) 85-94; DOI: 10.3221/IGF-ESIS.40.08 92 D ISCUSSION AND CONCLUSIONS his study aimed to assess the effect of obesity and exercise on bone biomechanics and biochemical measurements and investigate the potentially beneficial role of exercise. For this purpose, a well-established mouse model of HFD–induced obesity was used [7, 15]. More specifically, mice were randomly assigned in three groups, namely control (group A), HFD with no exercise (group B) and HFD with exercise (group C). Body mass and relevant biochemical parameters were measured for the duration of the study (i.e. 37 weeks). During the first 28 weeks of the experimental protocol groups B and C were exposed to exactly the same conditions. Indeed, exercise was not introduced to the protocol until the end of the 28 th week. This means that analysing the results for the first 28 weeks enables only the assessment of the effect of HFD on body mass and the biochemical profile of the animals. Any difference between groups B and C up to week 28 could be attributed to variations that are inherent in in- vivo testing. As expected HFD had a significant effect on body mass [15]. More specifically, the animals that received HFD gradually increased their body mass relatively to control with statistically significant differences appearing during the 28 th week of the study. With regards to the biochemical measurements, HFD appears to consistently lead to higher levels of cholesterol (T-CHOL and HDL-C). One way repeated measures ANOVA for group C indicates that the introduction of exercise is followed by some changes, including a drop in body mass, increase in TG levels etc. However, in most cases these changes are not substantial enough to make group C significantly different compared to group B (Fig. 3). The fact that the introduction of exercise didn’t appear to lead to substantial changes in body mass and the biochemical profile of group C could be attributed to the specific exercise protocol employed in this study and its relatively limited duration (i.e. 9 weeks). Indeed, there is evidence in literature that exercise of different intensity, frequency and duration can lead to different results in animal HDL- induced obesity models [20]. The levels of adiponectin were also not affected by HFD or exercise. Adiponectin has been reported in literature to have a positive effect on bone properties by activating osteoblastogenesis and suppressing osteoclastogenesis, thus leading to increased bone mass [22]. However, the fact that the results of the present study didn’t reveal any statistically significant difference between groups with regards to adiponectin levels means that no relevant conclusion can be drawn. So far, the effect of exercise and diet on bone strength has been either inferred based on non-invasive measurements and/or computer modelling [23] or directly measured through in-vitro testing [19, 20, 24, 25]. The most commonly used testing techniques are three point bending and torsion which are typically used to measure the maximum sustained force [25] or moment [20], respectively as a measure of strength. These studies have indicated that obesity and exercise can affect both the structure and also the mechanical characteristics of bones [19, 23, 24]. Assessing ultimate stress along with the maximum sustained force enables separating the effect of changes in geometry from changes in the actual material properties of bone tissue [19, 24]. In order to enable the calculation of ultimate stress from the measured fracture force, the cross-section of the specimens was considered to be elliptical with constant thickness [21]. This simplification was deemed to be necessary considering the small size of the samples. Indeed, the longest cross-sectional distance was smaller than 3 mm. The results from biomechanical testing indicated that the morphology and mechanical strength of femurs was significantly affected by diet and exercise. In terms of morphology, HFD appears to increase the external dimensions of femur regard- less of the exposure to exercise. However, the group that received HFD but was not exposed to exercise (group B) also appeared to have significantly lower bone thickness compared to the other two groups. These findings indicate that exercise tends to limit the HFD-induced loss of bone mass by increasing the thickness of the femurs’ cortical shell. Inte- restingly though, this positive effect of exercise was not translated into increased ultimate stress. Hence, both groups that received HFD had significantly lower ultimate stress relatively to control. No statistically significant difference was found in terms of fracture force or total energy. The aforementioned findings are in agreement with observations linking obesity to the loss of bone mass and osteopenia [7, 8]. High-fat diets in particular have been found to reduce the ability for calcium absorption with possible adverse effects on bone mineralization in growing animals [8]. An investigation of correlations between biomechanical parameters, body mass and biochemical measurements that was focused only on the mice that received HFD (i.e. groups B and C) revealed strong positive associations between fracture force and serum glucose and body mass. More specifically, the femurs of mice that, at the end of the protocol, had higher body mass or glucose levels were found to be stronger compared to mice with lower body mass or glucose levels. T